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Interactions between N-Ethylmaleimide-sensitive factor and GluA2 contribute to effects of glucocorticoid hormones on AMPA
receptor function in the rodent hippocampus.

Journal

Hippocampus

Volume | Issue number

26 | 7

Pages (from-to)

848-856

Document type

Article

Faculty

Faculty of Science (FNWI)

Institute

Swammerdam Institute for Life Sciences (SILS)

Abstract

Glucocorticoid hormones, via activation of their receptors, promote memory consolidation, but the exact underlying mechanisms
remain elusive. We examined how corticosterone regulates AMPA receptor (AMPAR) availability in the synapse, which is important
for synaptic plasticity and memory formation. Peptides which specifically block the interaction between N-Ethylmaleimide-Sensitive
Factor (NSF) and the AMPAR-subunit GluA2 prevented the increase in synaptic transmission and surface expression of AMPARs
known to occur after corticosterone application to hippocampal neurons. Combining a live imaging Fluorescence Recovery After
Photobleaching (FRAP) approach with the use of the pH-sensitive GFP-AMPAR tagging revealed that this NSF/GluA2 interaction
was also essential for the increase of the mobile fraction and reduction of the diffusion of AMPARs after treating hippocampal
neurons with corticosterone. We conclude that the interaction between NSF and GluA2 contributes to the effects of corticosterone
on AMPAR function.

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